D-Lactic Acid Metabolism and Control of Acidosis
Aims of this work were to determine: 1) Influence of the presence of D-lactate or acidity on neurological disturbances; 2) Effectiveness of parenteral NaHCO3 therapy in correcting cerebrospinal acidity and DLA; 3) Prevalence of DLA in diarrheic lambs and fecal D-lactate thresholds; 4) Effectiveness of malate in preventing DLA.
The methodological tools consisted of animal models (calves and lambs): 1) Advanced surgical procedure in calves for long-lasting atlanto-occipital catheterizations; 2) Intravenous infusions of acids to experimentally induce acidosis; 3) Intravenous NaHCO3 therapies; 4) Sampling of cerebrospinal fluid (CSF), blood, urine and feces from experimental / treated calves or diarrheic lambs for blood gas analysis, and D-lactate separation by chromatography.
D-lactate entered the central nervous system (> 2 mmol/L) from the circulation following experimentally induced D-lactatemia (> 5 mmol/L) and was responsible for neurological disturbances which correlated (r = 0.9, P < 0.05) with both CSF and serum D-lactate concentrations. A zenith of neurological disturbances, ataxia was evident when D-lactate concentration exceeded 12 mmol/L (CSF) and 26 mmol/L (serum), however, a nadir of acidosis (pH 6.9) caused by HCl infusions produced only mild neurological disturbances (P < 0.05). Therapeutic NaHCO3 infusions did not result paradoxical CSF acidosis, but supportive in correcting (P < 0.05) acidosis (ÄpH + 0.11) and D-lactatemia in calves.
In lambs, metabolic acidosis following a range of mild to severe diarrhea was observed with a corresponding range of D-lactate concentrations in both serum (< 0.05?24.0 mmol/L) and feces (< 0.05?31.0 mmol/L). D-lactate was absorbed into the circulation when the fecal D-lactate concentration exceeded 10.2 mmol/L (threshold). In calves, moderate oral use of malate produced a > 50% (P < 0.05) decrease in fecal and serum D-lactate concentrations suggesting prebiotic properties to prevent DLA.
This dissertation answers the critical questions about the onset of neurological signs in D-lactic acidosis, and advances the current knowledge on the metabolism of D-lactate, the prevention and treatment of acidosis.
Advisor:Zello, G. A.; Brocks, D. R.; Chilibeck, P. D.; Bandy, B.; Hamilton, D. L.; Naylor, J. M.; Paterson, P. G.
School:University of Saskatchewan
School Location:Canada - Saskatchewan
Source Type:Master's Thesis
Keywords:d lactatic acidosis incidence treatment prebiotic neuropathy
Date of Publication:04/21/2009